Kaplan Cynthia G., MD Color Atlas of Gross Placental Pathology

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38 Chapter 3 Umbilical Cord

Figure 3.23. Cord

insertion into the

free membranes

(velamentous

insertion) occurs

in about 1% of

deliveries. The

vessels must be

carefully examined

for integrity

and extent of

membranous

passage. Old

hemorrhage behind

the membranes is

sometimes found

where the cord

attaches.

Figure 3.24.

Intrapartum rupture

of a velamentous

vessel occurred in

this case (arrow)

supported by

maternal history and

neonatal anemia.

This infant survived.

Hemorrhage from a

ruptured vessel is

usually found in the

sub-amniotic region.

Vessels may also be

torn after the infant

has been born,

during placental

delivery. While this

has no clinical

signiﬁcance, it should

be noted since

complete historical

information may not

be available at the

time of placental

examination.

Insertion 39

Figure 3.25. Despite the close proximity of the cord insertion and velamentous

vessels to the site of membrane rupture in this vaginal delivery, no vascular

disruption occurred. Vessels overlying the cervical os (vasa previa) are at the

greatest risk of tearing and causing catastrophic fetal blood loss. Velamentous

vessels may also be compressed during labor. There is a ﬂeck of calcium in one

velamentous vessel which is likely old thrombosis (arrow).

The vessels in the cord may separate before it reaches the surface

(furcate). The unattached surface amnion may also attach to the cord

several centimeters before the cord reaches the placental surface (Figure

3.26 to Figure 3.29).

Figure 3.26. This

cord divides into

vessels which lose

their protective

covering of

Wharton’s jelly

above the surface of

the placenta. Such

furcate insertions

will have the risks

attendant to

velamentous vessels.

40 Chapter 3 Umbilical Cord

Figure 3.27. At times the cord is par-

tially encased by a fold of amnion at its

placental end, a “chorda” or amniotic

web. This cord is minimally furcate with

a web of amnion enclosing the vessels. A

clamp mark is present (arrow).

Figure 3.28.

Amniotic webs are

very common and

can extend for

several centimeters

up the cord. They

may be loose or

relatively tight and

bind the cord to the

fetal surface of the

placenta. If the

amnion is largely

detached from the

chorion, a web is

likely.

Infections 41

Figure 3.29. A long

tight amniotic web is

present. Webs may

limit the mobility of

the cord, potentially

compromising blood

ﬂow. There is also

subamniotic

hemorrhage.

Although bleeding

from vessels between

the amnion and

chorion is usually

an artifact arising

during placental

delivery, it is

common when webs

are present,

suggesting abnormal

stress in this area.

Infections

The cord inﬂammation seen with most ascending membranous infections

(see page 56) is usually not recognizable grossly. Candida is an excep-

tion and shows characteristic micro abscesses on the cord surface (Figure

3.30, Figure 3.31). This infection may cause a rash on the infant at birth.

Figure 3.30.

Scattered yellow to

white 2-mm to 3-mm

plaques on the

cord are virtually

pathognomonic of

Candida funisitis.

They are not seen

elsewhere on

the placental

membranes. There is

usually an associated

chorioamnionitis.

42 Chapter 3 Umbilical Cord

Figure 3.31. (A) Histologically Candida funisitis shows micro abscesses just

under the cord surface. These are ﬁlled with necrotic debris, in which it is difﬁ-

cult to identify organisms, (B) numerous fungal pseudohyphae and yeasts are

present on methenamine silver stain.

Infections 43

Figure 3.32. Necrotizing funisitis represents a chronic inﬂammatory process in

the umbilical cord, apparently infectious in origin. There is calciﬁcation sur-

rounding the vessels leading to an extremely rigid cord. This is at times visible

along the length as a white stripe.

Figure 3.33. Cross-section of a cord with necrotizing funisitis shows white bands

suggesting diffusion rings surrounding each of the three vessels. These are com-

posed of necrotic inﬂammatory cells and calciﬁcation.

It is more likely to cause sepsis in premature infants. The “barber-pole”

conﬁguration of chronic necrotizing funisitis is felt to represent a chronic

and sometimes healed intra-uterine infection with organisms of low vir-

ulence (Figure 3.32, Figure 3.33).

44 Chapter 3 Umbilical Cord

Ulceration

Loss of Wharton’s jelly with ulceration of the cord surface is uncommon,

but the associated infants may have signiﬁcant problems. It is usually

related to bile or meconium exposure (Figure 3.34).

Figure 3.34. Ulceration of the cord occurs in some cases of upper gastrointesti-

nal tract atresia. This infant had proximal jejunal atresia. The exposed vessels

may hemorrhage leading to fetal compromise or death. The intestinal obstruc-

tions are located below the Ampulla of Vater as the bile, appears to be etiologic.

Ulceration also may occur with longstanding meconium exposure.

Fetal Membrances and Surface

Layers

The peripheral membranes and fetal placental surface are continuous,

and most processes are seen in both. The layer of membrane closest

to the fetus is amnion. External is the chorion, which is minimal on the

peripheral membranes and more extensive on the disk. The remnant of

the yolk sac lies between the amnion and chorion (Figure 4.1). The

chorion is continuous with all the villous tissue. There is close proximity

of the surface membranes to the maternal blood of the intervillous space,

while the peripheral membranes abut the decidua and its blood vessels.

This relationship permits maternal cells access to the membranes.

Subchorionic Fibrin and Hemorrhage

Deposits of ﬁbrin from the maternal circulation and thrombosis are

common beneath the fetal surface.As pregnancy progresses, the amounts

of these materials generally increase (Figure 4.2, Figure 4.3). Subchori-

onic thrombi eventually become compacted ﬁbrin. The quantity of sub-

chorionic ﬁbrin has been associated with fetal activity. Large nodular

subchorionic hematomas, sometimes called “Breus moles,” are seen in

both liveborns and spontaneous abortions (Figure 4.4). Unusually thick

layers of subchorionic hemorrhage can be associated with chronic bleed-

ing and prematurity (Figures 4.5).

Extrachorial Placentation

The membranes normally insert at the peripheral margin of the villous

tissue which is usually the outer limit of the vascular plate. Extrachorial

placentation exists when villous tissue extends outward beyond the vas-

cular plate. This takes two forms, circummargination and circumvallation

(Figure 4.7). In circumvallation there is a redundant, doubled-back mem-

brane fold with enclosed debris and old hemorrhage at the point of mem-

brane insertion (Figure 4.8, Figure 4.9). In circummargination there is a

46 Chapter 4 Fetal Membrances and Surface

Figure 4.1. The yellow 4-mm nodule is the calciﬁed remnant of the yolk sac. It

lies free between the amnion and chorion. These are quite commonly found in

normal term placentas and are usually located near the edge of the placenta or

in the membranes.

Figure 4.2. Subchorionic ﬁbrin tends to increase with gestational age, although

it is quite variable. An immature placenta shows minimal subchorionic ﬁbrin,

leading to the deep blue surface coloration commonly seen. The minimal ﬁbrin

present appears as tiny nodules under the fetal surface (arrow).

Extrachorial Placentation 47

Figure 4.3. Abundant ﬁbrin deposition is often a striking feature of the fetal

surface in term placentas. It is composed of larger nodular aggregates of ﬁbrin

and old subchorionic hemorrhages which have lost their pigmentation. It may

become quite dense, as seen in this term placenta. When possible, histologic sec-

tions should not be taken from areas with thick ﬁbrin. Inﬂammatory processes

are often masked in such areas. An increased number of early amniotic sac infec-

tions will be diagnosed if thin, more transparent surface areas are sampled.

Figure 4.4. Extensive thick clot and hemorrhage undermine the fetal surface in

this case, a change which may be seen as early as midtrimester. The membranes

are discolored from hemosiderin pigment, and the amniotic ﬂuid may be thick

and brown. Placentas such as this are sometimes called “Breus moles.”